In The News
The Covid-19 pandemic has pushed telehealth — the remote provision of health care resources, tools, and consultation, usually via digital technologies — from the backwaters of medicine to its leading edge.
Though novel to some health care providers, and considered impractical by others, telehealth will likely endure — and become even more appealing — after the Covid-19 pandemic has faded away. We are concerned that this crisis-driven acceleration in the adoption of virtual visits and use of algorithmic tools will have uncertain implications for the equitable distribution of health resources and will widen racial and class-based disparities in health.
The changes that have made possible the wider use of telehealth appear to be temporary. For instance, health insurers, who once declined to fully reimburse virtual visits to physicians, nurse practitioners, and other health providers, are now making exceptions expressly tied to the nature of the pandemic. Yet research and theory from the social sciences on institutional change would predict that there may not be a clear-cut return to “normal” once this crisis is over.
The adaptation to Covid-19 has realigned the power and positions of physicians, nurses, insurance companies, hospitals, and telehealth startups in providing health services to different communities. Providers are establishing new policies and automated systems around triage, virtual visits, and infection control that may become taken-for-granted work routines going forward. Such practices may be laying the foundation for opportunism in the expansion of telehealth markets above and beyond their value in treating disease and saving lives by allowing compensation for unnecessary visits.
For some time, technology companies have sought to disrupt the health sector with algorithms and other patient-centered digital innovations. These companies are now rushing to consolidate their positions before the opportunities presented by the pandemic abate.
Some providers and hospitals, attracted by potential reductions in cost and in potential improvements in patients’ health outcomes, were early adopters of virtual visits and other telehealth technologies. With the emergence of Covid-19, providers who had once been prudently looking for an evidence-based way to add value to their practices have been pushed into rapidly developing telehealth strategies to keep their practices afloat. Academic medical centers that had previously piloted telehealth as a strategy to expand their referrals or to decrease readmissions are now leveraging this infrastructure to more intentionally maintain contact with patients who have been seen in their outpatient offices.
There’s no question that the expansion of telehealth could be a force for good. These changes may save lives during this crisis by keeping patients out of health care settings where exposure to Covid-19 may be high. In the post-pandemic era, they could provide greater access and convenience for some patients. But they could also worsen health disparities down the road if not implemented carefully.
In its earliest days, one of telehealth’s missions was to ensure greater access to health care services by populations that otherwise would go without proper or timely care and consultation, such as those who are incarcerated or who live in rural areas. Now it is being used as a tool to supplant in-person visits and expand patient markets, partly in response to consumer demand for convenience and efficiency. This emphasis on expanding patient markets and responding to well-resourced consumers’ demand may put marginalized groups with poor health, no health insurance, or few digital resources at risk.
A market-driven, consumer-centered vision of telehealth could have negative implications for marginalized groups that already face discrimination during in-person medical encounters. Marginalized racial and ethnic minorities are more likely to report discrimination within health care settings, influencing their willingness to trust providers and seek medical attention early.
Discrimination and mistrust could be magnified in virtual doctor-patient encounters, in which patients may not feel they can fully communicate and providers may be less mindful of guarding against implicit bias based on attributes such as race, ethnicity, or educational status.
The potential for racism and class bias to be encoded into telehealth algorithms is also worrisome. Predictive tools are imperfect — although they may be able to predict average patterns across groups, they can neither fully account for the complexity of individuals nor incorporate subtle variables that may assist in the identification and treatment of disease. While doctors misuse of these algorithms is mitigated by clinical judgement and training, a patients’ uninformed use of such algorithms in lieu of seeking professional medical advice could be harmful. This is particularly true of patients who belong to social groups underrepresented in algorithmic data.
Hospitals, insurers, policymakers, and health care professionals must carefully consider how the telehealth policies and routines they implement might have durable — and potentially harmful — reverberations. Research into the costs and benefits of specific telehealth applications at the individual and population levels is essential.
Institutional policies created during this pandemic will have long-lasting consequences on health disparities. We must work to ensure they are net positive.
Matthew Clair is a sociologist and assistant professor of sociology at Stanford University. Brian W. Clair is an orthopedic surgeon at Lahey Hospital and Medical Center in Burlington, Mass. Walter K. Clair is a cardiologist, professor of medicine at Vanderbilt University Medical School, and executive medical director of the Vanderbilt Heart and Vascular Institute.
We are making headway (maskway?) here in the United States, with more consensus that masks are key. Collectively, we can drive transmission down big time by wearing them. But if we accept that the average person—talking about myself here—can’t wear a mask 24/7, then we need to make sure we have the best masks possible, and that we wear them when it is most critical.
Masks are important because they both block transmission to others and protect the wearer. They don’t do either perfectly—the better the mask, the better it works—but perfect is the enemy of good enough to keep the R0 below one. So, masks are better than no masks. That’s the most important point.
We would greatly benefit from better masks. Folded up T-shirts work, but the better the mask, the less the viral transmission. This is especially true for essential workers and those at high risk of severe disease. Higher filtration masks are key.
How do we get better masks? This will have to happen either through the federal government — which seems unlikely, unless officials invoked the Defense Production Act — or through the private sector. Investors and companies should be racing toward making these, with a huge market opportunity in addition to the massive public health benefit.
Masks are not just needed to stop Covid-19 cases, hospitalizations, and deaths. They are also our ticket to actually reopening safely, getting back to work, and doing the things that we love to do. Without a vaccine, masks are our next, most pragmatic and achievable step to burning out the epidemic.
Masking is not an all or nothing behavior, either. I keep seeing people running outside alone with masks on, yet not masking indoors while socializing with friends and family. When you mask is almost as important as if you mask. If people can only realistically mask for X number of hours, then they must do so when transmission risk is highest.
This means masking indoors. This may very well mean masking around family or relatives as well, especially if they are in vulnerable risk groups and you live in a high-transmission area. In addition, this means masking while riding public transportation and at work.
Masking while alone in your car or when you are on a walk by yourself or for the second you pass by someone on the street is less useful. Your mask here likely won’t do too much as your risk of transmission is already very low.
So in short: Masks work, better masks work better, and masking during high-risk transmission situations matters more than during those which are low risk. Lastly, don’t shame those not wearing a mask. It won’t work. A genuine conversation may go further—but keep your own mask on.
Hundreds of international scientists are urging the World Health Organisation to revise its guidelines about the airborne transmission of coronavirus.In an open letter, 239 experts from 32 countries point to new research that shows an infected person exhales airborne virus droplets when breathing and talking that can travel further than the current 1.5m social distance requirement.The research, from Queensland University of Technology, shows poor ventilation in public buildings, workplace environments, schools, hospitals, aged care homes, or activities such as singing, contribute to viral spread.
Improved ventilation is vital for protecting against airborne infection transmission, the scientists warned.Led by Professor Lidia Morawska, the experts say the 1.5 metre social distancing rule is not far enough.”Studies by the signatories and other scientists have demonstrated beyond any reasonable doubt that viruses are exhaled in microdroplets small enough to remain aloft in the air and pose a risk of exposure beyond 1m to 2m by an infected person,” Professor Morawska said.”At typical indoor air velocities, a five-micron droplet will travel tens of metres, much greater than the scale of a typical room while settling from a height of 1.5m above the floor.”
Signatories to the appeal come from many disciplines including different areas of science and engineering, including virology, aerosol physics, flow dynamics, exposure and epidemiology, medicine, and building engineering.
Professor Morawska said there are affordable simple measures that can be taken to lessen the risk of airborne infection in buildings:
- Provide sufficient and effective ventilation (supply clean outdoor air, minimise recirculating air) particularly in public buildings, workplace environments, schools, hospitals, and aged care homes.
- Supplement general ventilation with airborne infection controls such as local exhaust, high efficiency air filtration, and germicidal ultraviolet lights.
- Avoid overcrowding, particularly in public transport and public buildings.
“Hand-washing and social distancing are appropriate, but it is view, insufficient to provide protection from virus-carrying respiratory microdroplets released into the air by infected people,” she said.The appeal is to be published in the journal Clinical Infectious Diseases.
The reports seemed to take doctors by surprise: The “respiratory” virus that causes Covid-19 made some patients nauseous. It left others unable to smell. In some, it caused acute kidney injury.
As the pandemic grew from an outbreak affecting thousands in Wuhan, China, to some 10 million cases and 500,000 deaths globally as of late June, the list of symptoms has also exploded. The Centers for Disease Control and Prevention constantly scrambled to update its list in an effort to help clinicians identify likely cases, a crucial diagnostic aid at a time when swab tests were in short supply and typically took (and still take) days to return results. The loss of a sense of smell made the list only in late April.
“For many diseases, it can take years before we fully characterize the different ways that it affects people,” said nephrologist Dan Negoianu of Penn Medicine. “Even now, we are still very early in the process of understanding this disease.”
What they are understanding is that this coronavirus “has such a diversity of effects on so many different organs, it keeps us up at night,” said Thomas McGinn, deputy physician in chief at Northwell Health and director of the Feinstein Institutes for Medical Research. “It’s amazing how many different ways it affects the body.”
One early hint that that would be the case came in late January, when scientists in China identified one of the two receptors by which the coronavirus, SARS-CoV-2, enters cells. It was the same gateway, called the ACE2 receptor, that the original SARS virus used. Studies going back some two decades had mapped the body’s ACE2 receptors, showing that they’re in cells that line the insides of blood vessels — in what are called vascular endothelial cells — in cells of the kidney’s tubules, in the gastrointestinal tract, and even in the testes.
Given that, it’s not clear why the new coronavirus’ ability to wreak havoc from head to toe came as a surprise to clinicians. Since “ACE2 is also the receptor for SARS, its expression in other organs and cell types has been well-known,” said Anirban Maitra of MD Anderson Cancer Center, who led a study mapping the receptor in cells of the GI tract. (Maitra is an expert in pancreatic cancer and, like many scientists this year, added Covid-19 to his research.)
Infecting cells is only the first way SARS-CoV-2 wreaks havoc. Patients with severe Covid-19 also suffer a runaway inflammatory response and, often, clot formation, said infectious disease physician Rochelle Walensky of Massachusetts General Hospital. That can cause symptoms as different as a lack of blood flow to the intestines and the red, inflamed “Covid toe.”
“We’ve had five cases of patients who’ve had to have their gut removed,” Walensky said. “You see these cases and you say, wait a minute; the virus is doing this, too? It has definitely been keeping us on our toes.”
Venky Soundararajan had a hunch that the extent of ACE2 distribution throughout the body was lying in plain sight. The co-founder and chief scientific officer of nference, which uses artificial intelligence to mine existing knowledge, he and his colleagues turned their system into a hunt for ACE2 knowledge. Combing 100 million biomedical documents from published papers to genomic and other -omics databases, they uncovered multiple tissues and cell types with ACE2 receptors, they reported last month in the journal eLife.
They also calculated what percent of each cell type expresses “reasonable amounts” of ACE2, Soundararajan said. On average, about 40% of kidney tubule cells do, and in a surprise for a “respiratory” virus, cells in the GI tract were “the strongest expressors of ACE2 receptors,” he said.
The data mining found that ACE2 is also expressed in the nose’s olfactory cells. That’s not a new finding per se — the inference system found it in existing databases, after all — but it hadn’t been appreciated by scientists or clinicians. It explains the loss or altered sense of smell that Covid-19 patients experience. Its importance became clear earlier this month when scientists at the Mayo Clinic and inference reported that loss of a sense of smell is “the earliest signature of Covid-19,” appearing days before a positive swab test.
That study, using health records of 77,167 people tested for Covid-19, showed how the assumption that infection would first and foremost cause respiratory symptoms was misplaced. In the week before they were diagnosed, Covid-19 patients were 27 times more likely than people who tested negative for the virus to have lost their sense of smell. They were only 2.6 times more likely to have fever or chills, 2.2 times more likely to have trouble breathing or to be coughing, and twice as likely to have muscle aches. For months, government guidelines kept people not experiencing such typical signs of a respiratory infection from getting tested.
Faced with a disease the world had never seen before, physicians are learning as they go. By following the trail of ACE2 receptors, they are more and more prepared to look for, and treat, consequences of SARS-CoV-2 infection well beyond the obvious:
Gut: The coronavirus infects cells that line the inside of the large and small intestine, called gut enterocytes. That likely accounts for the diarrhea, nausea, and abdominal pain that about one-third of Covid-19 patients experience, said MD Anderson’s Maitra: “The GI symptoms reflect physiological [dysfunction] of cells of the lower GI tract.”
Why don’t all patients have GI symptoms — or indeed, the whole panoply of symptoms suggested by the near ubiquity of ACE2 receptors? For those with mild to moderate Covid-19, “the infectious load in the GI tract may simply not be sufficient to cause symptoms,” Maitra said.
Kidney: The cells lining the tubules that filter out toxic compounds from the blood are rife with ACE2 receptors. Last month, scientists studying 1,000 Covid-19 patients at a New York City hospital reported that 78% of those in intensive care developed acute kidney injury.
Smell: An analysis of 24 studies with data from 8,438 Covid-19 patients from 13 countries found this month that 41% had lost their sense of taste or smell, or both. That shouldn’t be surprising, said Fabio Ferreli of Humanitas University in Milan: “Perhaps the highest levels of ACE2 receptors are expressed in cells in the nasal epithelium.” The sensory loss isn’t due to nasal inflammation, swelling, or congestion, he said, “but to direct damage” to these epithelial cells. Loss of smell also impacts taste, but the virus may also have a direct effect on taste: The nference analysis found high levels of the ACE2 gene in tongue cells called keratinocytes, which contribute to the sense of taste.
There is another implication of the high expression of ACE2 in olfactory epithelium cells, scientists at Johns Hopkins concluded in a paper posted to the preprint site bioRxiv last month: ACE2 levels in the olfactory epithelium of the upper airways that are 200 to 700 times higher than in the lower airways might explain the virus’s high transmissibility. It was weeks before experts recognized that the virus could spread from person to person.
Lungs: This is where a respiratory virus should strike, and SARS-CoV-2 does. The lungs’ type II alveolar cells — among other jobs, they release a compound that allows the lungs to pass oxygen to the blood and take carbon dioxide from it — are studded with ACE2 receptors. Once infected with the coronavirus, they become dysfunctional or die, and are so swarmed by immune cells that this inflammatory response can explode into the acute respiratory distress syndrome (ARDS) that strikes many patients with severe Covid-19, Walensky said.
There is new evidence that the virus also attacks platelet-producing cells, called megakaryocytes, in the lungs. In a study published on Thursday, pathologist Amy Rapkiewicz of NYU Winthrop Hospital found something she had “never seen before”: extensive clotting in the veins and other small blood vessels of patients’ hearts, kidneys, liver, and lungs. She suspects that the platelets produced by infected megakaryocytes travel through the bloodstream to multiple organs, damaging their vasculature and producing potentially fatal clots. “You see that and you say, wow, this is not just a ‘respiratory’ virus,’” Rapkiewicz said.
Pancreas: In April, scientists in China reported that there was higher expression of the gene for ACE2 in the pancreas than in the lungs. Genetic data are an indirect measure of ACE2 receptors themselves, but could have been a tip-off to physicians to monitor patients for symptoms there. As it happens, the Chinese researchers also found blood markers for pancreas damage in Covid-19 patients, including in about 17% of those with severe disease.
Heart: Patients with severe Covid-19 have a high incidence of cardiac arrests and arrhythmias, scientists at the Perelman School of Medicine at the University of Pennsylvania recently found. That’s likely due to an extreme inflammatory response, but there might be more direct effects of the coronavirus, too. A large team of European researchers reported in April that arrhythmia (including atrial fibrillation), heart injury, and even heart failure and pulmonary embolism might reflect the fact that ACE2 receptors are highly expressed in cells along the inside walls of capillaries. When these “vascular endothelial” cells become infected, the resulting damage can cause clots, MGH’s Walensky said, which in turn can cause Covid toe, strokes, and ischemic bowel (too little blood flow to the gut). Studies from around the world suggest that 7% to 31% of Covid-19 patients experience some sort of cardiac injury.
Gallbladder: Specialized cells in this organ, too, have high levels of ACE2 receptors. Damage to the gallbladder (like the pancreas) can cause digestive symptoms.
With the number of Covid-19 patients closing in on 10 million, physicians fervently hope the virus has no more surprises in store. But they’re not counting on it.
“I’ve seen patients every day during this crisis,” said Northwell’s McGinn. “There have been times when I’ve said, wait, the virus can’t do anything new — and then there’s a young woman with a stroke or an older man with myocarditis,” inflammation of the heart muscle. “I keep thinking I’m going to run out of material” for the teaching videos he does on Covid-19, “but it hasn’t happened.”